Based on this and on the fact that liver-specific SKO mice did not develop steatosis, the hepatic steatosis observed in the current study may not be directly related to the loss of a liver-specific seipin function but rather with the reduced amount of metabolically active adipose tissue [9,16], which was lower in the homozygous animals, potentially explaining the observed histopathological changes in the liver. Here, BSCL2 is linked to Hepatic steatosis.